| + |
CASP8 | up-regulates activity 
cleavage
|
BID |
0.872 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-59655 |
Asp60 |
GYDELQTdGNRSSHS |
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 9727492 |
Caspase-8 cleaves bid at aspartic acid residue 60 (asp60) cleavage of bid by casp8 releases its potent proapoptotic activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS, TNF-alpha Signaling |
| + |
Caspase 8 complex | up-regulates activity
cleavage
|
BID |
0.872 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256443 |
Asp60 |
GYDELQTdGNRSSHS |
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 9727492 |
Caspase-8 cleaves bid at aspartic acid residue 60 (asp60) cleavage of bid by casp8 releases its potent proapoptotic activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CSNK2A1 | up-regulates activity
phosphorylation
|
BID |
0.289 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250830 |
Ser64 |
LQTDGNRsSHSRLGR |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250831 |
Thr59 |
EGYDELQtDGNRSSH |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
CSNK2A2 | up-regulates activity
phosphorylation
|
BID |
0.289 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250978 |
Ser64 |
LQTDGNRsSHSRLGR |
Homo sapiens |
|
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250979 |
Thr59 |
EGYDELQtDGNRSSH |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
CSNK1A1 | up-regulates activity
phosphorylation
|
BID |
0.289 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250785 |
Ser64 |
LQTDGNRsSHSRLGR |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250786 |
Thr59 |
EGYDELQtDGNRSSH |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
CSNK2B | up-regulates activity
phosphorylation
|
BID |
0.289 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251053 |
Ser64 |
LQTDGNRsSHSRLGR |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251054 |
Thr59 |
EGYDELQtDGNRSSH |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
CSNK1E | up-regulates activity
phosphorylation
|
BID |
0.349 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250805 |
Ser64 |
LQTDGNRsSHSRLGR |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250806 |
Thr59 |
EGYDELQtDGNRSSH |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11583622 |
Here we report that Bid is phosphorylated by casein kinase I (CKI) and casein kinase II (CKII). Inhibition of CKI and CKII accelerated Fas-mediated apoptosis and Bid cleavage, whereas hyperactivity of the kinases delayed apoptosis. | These results suggest that residues S61, S64, and to a much lesser extent T58 are sites of phosphorylation of Bid. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
MTCH2 | up-regulates
binding, relocalization
|
BID |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-171773 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21295084 |
Mtch2/mimp and its role in bid recruitment may synergise with cl-induced mitosome formation to facilitate momp. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-165081 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20436477 |
Mtch2/mimp (mitochondrial carrier homologue 2/met-induced mitochondrial protein), a novel truncated bid (tbid)-interacting protein, is a surface-exposed outer mitochondrial membrane protein that facilitates the recruitment of tbid to mitochondria |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
Caspase-2 PIDDosome | up-regulates activity
cleavage
|
BID |
0.55 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262644 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20158568 |
Inactive caspase-2 monomers are recruited to the PIDDosome in response to certain cellular stresses. This results in dimerization and activation of caspase-2. Caspase-2 cleaves and activates Bid to induce MOMP eventually resulting in activation of executioner caspases by caspase-9-mediated cleavage. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HIF-1 complex | down-regulates quantity by repression 
transcriptional regulation
|
BID |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267457 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27692180 |
HIF-1 promotes glycolysis by transcriptionally upregulating GLUT1, GLUT3, HK1, and HK2. HIF-1 also suppresses oxidative phosphorylation by the upregulation of gene expression of BNIP3, BNIP3L, LDHA, and PDK1. In addition, HIF-1 can inhibit apoptosis by suppressing the expression of BID. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BID | up-regulates
binding
|
BAK1 |
0.812 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-92942 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12242151 |
We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome c. these data support a two-class model for bh3 domains: bid-like domains that activate bax, bak and bad-like domains that sensitize by occupying the pocket of antiapoptotic members. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-105210 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11175253 |
Activated tbid results in an allosteric activation of bak |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152992 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17289999 |
We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome c. these data support a two-class model for bh3 domains: bid-like domains that activate bax, bak and bad-like domains that sensitize by occupying the pocket of antiapoptotic members. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
BID | up-regulates
binding
|
BAX |
0.817 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-152929 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17289999 |
We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome cthe first alfa helix of bax plays a necessary role in its ligand-induced activation by the bh3-only proteins bid and puma |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-92945 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12242151 |
We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome cthe first alfa helix of bax plays a necessary role in its ligand-induced activation by the bh3-only proteins bid and puma |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73902 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10629050 |
Bid, a bh3-domain-only protein which interacts with bax, was able to trigger a conformational change in bax. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-131442 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15574335 |
We find short peptides representing the alpha-helical bh3 domains of bid or bim are capable of inducing oligomerization of bak and bax to release cytochrome cthe first alfa helix of bax plays a necessary role in its ligand-induced activation by the bh3-only proteins bid and puma |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS, TNF-alpha Signaling |
| + |
BID | up-regulates activity 
|
CYCS |
0.574 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-59224 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9727492 |
TBID induces first the clustering of mitochondria around the nuclei and release of cytochrome c. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
ER stress | up-regulates
|
BID |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-196944 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22492984 |
Exposure to stress results in the induction of bh3-only proteins, which neutralise the pro-survival proteins |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
BID | down-regulates activity
binding
|
BCL2L1 |
0.85 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209675 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 22464442 |
Overexpression of antiapoptotic proteins including Bcl-XL and/or Bcl-2 contributes to tumor initiation, progression, and resistance to therapy by direct interactions with proapoptotic BH3 proteins. Release of BH3 proteins from antiapoptotic proteins kills some cancer cells and sensitizes others to chemotherapy. Binding of Bcl-XL and Bcl-2 to the BH3 proteins Bad, Bid, and the three major isoforms of Bim was measured for fluorescent protein fusions in live cells using fluorescence lifetime imaging microscopy and fluorescence resonance energy transfer. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
ITCH | down-regulates quantity by destabilization
ubiquitination
|
BID |
0.359 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271415 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 20392206 |
The ubiquitin ligase Itch mediates the antiapoptotic activity of epidermal growth factor by promoting the ubiquitylation and degradation of the truncated C-terminal portion of Bid |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TP53 | up-regulates quantity by expression
transcriptional regulation
|
BID |
0.497 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-140248 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 16151013 |
Bid is a p53 primary-response gene. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Mitochondrial Control of Apoptosis |
3.0
BID
- 
- 